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aa Step 2CK: Internal & Peds > Endocrinology- DM > Flashcards

Endocrinology- DM Flashcards

1
Q

Define Diabetes

A
  1. Fasting glucose ≥ 125 after on 2 occasions
  2. A randome glucose ≥ 200
  3. An A1c ≥ 6.5
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2
Q

Signs Symptoms of DM

A 
Polyuria
Polydipsia
Polyphagia
Decreased wound healing 
Candida Infections
Weight loss 
Blurry vision or Self Correcting Presbyopia
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3
Q

What antibodies are present in DM1?

A

Antibodies to glutamic acid decarboxylase (GAD)

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4
Q

What can falsely decrease HbA1c?

A

Hemmoglobinopathies: Sickle cell, G6PD, Thalassemia

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5
Q

What is the first treatment for DM2?

MOA, ADR, and contraindications?

A

BITx: Metformin + Lifestyle (weight loss, exercise, diet)

MOA: blocks gluconeogensis and intestine glucose absorption

ADR: lactic acidosis, B12 deficiency, weight loss

Contas: renal failure, alcoholics, ketoacidosis

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6
Q

DM2 Tx: Sulfanylureas

  • names
  • moa
  • adr
  • contraindications
A

Name: Glyburide, Glipizide. Analogues (Repaglinide, Nateglinide)

MOA: Block ATP-K channels of the pancreatic β cells → depolarization→ insulin secretion

ADR: Weight gain, hypoglycemia, disulfiram-like reaction

Contraindications: Severe cardiovascular, obesity, sulfa-allergy; Analogues: liver failure

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7
Q

DM2 Tx: DPP-4 inhibitors

  • names
  • moa
  • adr
  • contraindications
A

Names: -gliptin (sitagliptin, saxagliptin)

MOA: inhibiting the DPP-4 → less break down GLP-1 & GIP → insulin secretion, ↓ glucagon secretion, delayed gastric emptying

ADR: GI, risk pancreatitis, UTI (mild) , URI

Contras: Liver failure, kidney failure

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8
Q

DM2 Tx: SGLT2 inhibitors

  • names
  • moa
  • adr
  • contraindications
A

Names: -glifozin (empaglifozin, dapaglifozin)

MOA: inhibition of SGLT-2 in the PCT of kidney → ↓ glucose reabsorption → glycosuria and polyuria

ADR: UTI (significant), fungal vaginitis, dehydration, DKA

Contras: CKD, recurrent UTI.

use after 2-3 other oral dont work

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9
Q

DM2 Tx: Thiazolidinesiones

  • names
  • moa
  • adr
  • contraindications
A

Name: -glitazones (Pioglitazone, Rosiglitazone)

MOA: activation PPARγ → ↑ transcription of genes → ↑ adiponectin and insulin sensitivity → ↑ storage of fatty → ↓ free fatty acids → ↑ glucose utilization and ↓ hepatic glucose production

ADR: Weight gain, osteoporosis, risk of heart failure, edema & fluid retention.

Contras: no clear benefit; CHF; Liver failure

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10
Q

DM2 Tx: GLP-1 agonist

  • names
  • moa
  • adr
  • contraindications
A

Names: -tide (exenatide, liraglutide); semaglutide (first oral GLP agonist )

MOA: Bind to the GLP-1 receptors → ↑ insulin secretion, ↓ glucagon secretion, slow gastric emptying (↑ feeling of satiety, ↓ weight)

ADR: GI (slow gastric motility), weight loss, Pancreatitis

Conrats: symptomatic GI, Hx or FHx of pancreatitis or cancer

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11
Q

DM2 Tx: Alpha glucosidase inhibitors

  • names
  • moa
  • adr
  • contraindications
A

Names: acarbose, miglitol

MOA: Inhibit alpha-glucosidase → delayed and ↓ intestinal glucose absorption (post prandial control)

ADR: Flatus, diarrhea, abd pain,

Contras: IBD, malabsorption

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12
Q

Characteristics of insulin: rapid acting

  • names
  • onset
  • peak
  • duration
  • application
A

Names: Lispro, Aspart, glulisine (LAG)

Onset: 5-15 min
Peak: 1hr
Duration: 3-4 hrs

Application: basal bous; sliding scale

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13
Q

Characteristics of insulin: short acting

  • names
  • onset
  • peak
  • duration
  • application
A

Name: Regular

Onset: 30-60min
Peak: 2hrs
Duration: 6-8hrs

Application: hyperglycemic emergency (only IV insulin), insulin pumps, sliding scale

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14
Q

Characteristics of insulin: intermediate acting

  • names
  • onset
  • peak
  • duration
  • application
A

Name: NPH (Neutral protamine Hegedron)

Onset: 2-4 hrs
Peak: 6-7hrs
Duration: 10-16hrs

Application: glucocorticoid hyperglycemia, resistant DM2,

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15
Q

Characteristics of insulin: Long acting

  • names
  • onset
  • peak
  • duration
  • application
A

Names: glargine, detemir, degludec

Onset: 1-4 hrs
Peak: Flat- no peak
Duration: 24-36hrs

Application: Basal bolus regiment

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16
Q

Time adjustment for NPH and regular insulin:

7am glucose issue
12pm glucose issue
5pm glucose issue
9pm glucose issue

A

To correct a 7am problem adjust NPH at dinner the night before.

To correct 12pm: adjust Regular morning dose

To correct 5pm: adjust NPH morning dose

To correct 9pm: adjust Regular dinner dose.

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17
Q

Somogyi Effect

A

Too much insulin at dinner –> overnight hypoglycemia –> morning release stress hormone –> 7am high glucose.

Tx: decrease evening insulin

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18
Q

Dawn phenomenon

A

Hyperglycemia caused by growth hormone early in the am.
Elevated 7am glucose no overnight hypoglycemia.

Tx: increase evening glucose

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19
Q

What is DKA?

A

Diabetic Ketoacidosis is an acute hyperglycemic, hyperosmolar state typically in type 1 diabetics with metabolic acidosis (due to hepatic ketone production), and hyperkalemia.
Deadly without treatment.

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20
Q

What is HHS/NKHS

A

Non ketotic hyperglycemic hyperosmolar Syndrome occurs only in type 2 diabetics at much higher glucose levels. There is no ketones or acidosis due to small levels of insulin production.

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21
Q

What signs/ symptoms are specific to DKA?

A 
Polyuria 
Polydipsia
Volume depletion 
Neuro (AMS, lethargy, coma)
Rapid onset (< 24 h)
Abdominal pain 
Fruity odor(from exhaled acetone) 
Kussmaul respirations
Hyperkalemia w/ decreased total body K
Metabolic acidosis with anion gap
Low Bicarb
22
Q

What signs/ symptoms are specific to HHS?

A 
Polyuria/ Polydipsia
Recent weight loss
Nausea and vomiting 
Neuro (AMS, lethargy, coma)
Severly profound dehydration
Slower onset (over days)
Glucose >600
Normal Anion gap and Bicarb 
Increased risk seizure
23
Q

Tx DKA

A

first: Large volume fluids and short acting insulin

Replace K as levels approach normal.

Correct underlying cause.

24
Q

What is the mechanism of ketoacidosis in DKA?

A 
Insulin deficiency → 
↑ lipolysis → 
↑ free fatty acids → 
hepatic ketone production (ketogenesis) →
ketosis → 
bicarbonate consumption (as a buffer) → 
anion gap metabolic acidosis
25
Q

What is the mechanism of total potassium deficit in DKA?

A

Insulin deficiency →
hyperosmolality →
K shift out of cells + no insulin for K uptake →
intracellular K depleted & elevated blood K levels

26
Q

Which is the best measure of the severity in DKA?

A

Serum Bicarb (anion gap)

as anion gap increases risk of death increase, regardless of glucose level.

27
Q

What is the mortality rate of DKA and HHS?

A

DKA 10% with current treatment

HHS 50% if mental status change at start of treatment

28
Q

Tx HHS

A

Due to severe dehydration: FLUIDS FLUIDS FLUIDS

second: insulin and electrolyte replacement

29
Q

Health maintenance for diabetic patients

A 
Pneumococcal vaccine 
Annual eye exam (retinopathy)
ACE/ ARB if >140/90 or  +microalbuminuria 
Statin therapy LDL >100
Foot Exams 
Microalbuminuria test annually
30
Q

What are the most common long term complications of DM?

A 
Cardiovascular complications
Retinopathy
Nephropathy
Vascular disease
Neuropathy
Risk of infection
31
Q

Cardiovascular complications in DM

A

MI (most common cause of death in DM)
Silent MI (painless due to neuropathy)
Stroke
CHF

Goal BP <140/90, LDL <100

32
Q

Diabetic nephropathy

A

DM #1 cause of ERDS requiring HD

Microalbuminuria early disease
ACE/ ARB slow and prevent

33
Q

Diabetic retinopathy

A

DM leading cause of blindness due to microvascular damage.

Proliferative retinopathy: neovascularization and virtuous hemorrhages.

34
Q

Tx Diabetic retinopathy

A

Proliferative retinopathy is treated with pan retinal laser photocoagulation.

Vascular endothelial growth facto (VEGF) inhibitors treat severe retinopathy

35
Q

Diabetic neuropathy

A

Damage to microvasculature damages the vasa nervorum that surrounds peripheral nerves.

Neuropathy with pain: pregabalin, gabapentin, TCA

36
Q

Risk of infection in DM

A

WBC don’t function well in hyperglycemic environment. Decreses sensation and PAD cannot deliver WBC to site of early infection.

37
Q

What problems can result from diabetic neuropathy?

A 
Gastroparesis
Charcot Joints
Impotence
Cranial Nerve Palsies 
Orthostatic hypotension 
Foot injuries
38
Q

DM gastroparesis

A

Immobility os the bowel due to decreased ability to sense stretch of bowel walls.

Bloating, constipation, early satiety, vomiting

39
Q

Tx gastroparesis

A

Metoclopramide
erythromycin

Unresponsive: gastric pacemaker

40
Q

Charcot Joints

A

Joints of the foot and ankle deform secondary to lack of sensation. Pts may brake a bone and not feel it

41
Q

Impotence in DM

A

caused by vascular atherosclerosis and neuropathy

42
Q

Cranial nerve palsies in DM

A

Microvascular ischemia of Daniela nerves especially CN 3,4,6.

Facial nerve palsy simile to Bell palsy

43
Q

Orthostatic hypotension in DM

A

Arteries dont “clamp down” when the patients stands up and HR fails to increase

44
Q

How should you manage diabetic patients who are not allowed to eat because they are scheduled for surgery?

A

1/3 to 1/2 normal insulin dose.

Close glucose monitoring intra and post-op

45
Q

Beta blockers, hypoglycemia and diabetics?

A

BB mask classic symptoms of hypoglycemia which are caused by catecholamine release.
With Hx of previous MI, benefits outweigh risk of using a BB.

46
Q

What should be remembered before giving IV iodinated contrast to a diabetic?

A

DMs are prone to acute renal failure from IV iodine contrast. No concern with oral contract.
Weigh risks and benefits.

Administer IV fluids prior to contrast.

Decrease risk with acetylcystine and bicarb.

47
Q

IV iodinated contrast and metformin

A

Risk for lactic acidosis is acute renal failure were to accuse with IV contrast. Pts with advanced CKD or AKI should have metformin held before contrast and 48hrs after contrast.

48
Q

Hypoglycemia and DM

A

most common cause for hospitalization

MCC: inappropriate dose adjustment
Tx: glucose and/or glucagon

49
Q

Other causes of hypoglycemia

A

Insulinoma
Insuline autoimmune antibodies
Sulfonylurea Abuse
Serruptitious use of insulin/ suicide.

50
Q

When should a diabetic foot ulcer be imaged for osteomyelitis?

A 
Deep ( exposed bone, probe to bone)
Long standing ( >7-14 days)
Large (>2cm)
Elevated ESR/ C-reactive protein 
Adjacent soft tissue infection ( not always evident due to neuropathy and poor immune response)
51
Q

Elevated A1c with moral fasting glucose

A

post prandial hyperglycemia

52
Q

Management of post prandial hyperglycemia

A

Basial-Bolus insulin

Basal and Rapid acting

aa Step 2CK: Internal & Peds (71 decks)

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